Viuff B, Aasted B, Alexandersen S
Department of Pharmacology and Pathobiology, Agricultural University of Copenhagen, Frederiksberg C, Denmark.
J Virol. 1994 Apr;68(4):2720-5. doi: 10.1128/JVI.68.4.2720-2725.1994.
Neonatal mink kits infected with Aleutian mink disease parvovirus (ADV) develop an acute interstitial pneumonia with clinical symptoms and pathological lesions that resemble those seen in preterm human infants with respiratory distress syndrome and in human adults with adult respiratory distress syndrome. We have previously suggested that ADV replicates in the alveolar type II epithelial cells of the lung. By using double in situ hybridization, with the simultaneous use of a probe to detect ADV replication and a probe to demonstrate alveolar type II cells, we now confirm this hypothesis. Furthermore, Northern (RNA) blot hybridization showed that the infection caused a significant decrease of surfactant-associated protein C mRNA produced by the alveolar type II cells. We therefore suggest that the severe clinical symptoms and pathological changes characterized by hyaline membrane formation observed in ADV-infected mink kits are caused by a dysfunction of alveolar surfactant similar to that observed in respiratory distress syndrome in preterm infants. However, in the infected mink kits the dysfunction is due to the replication of ADV in the lungs, whereas the dysfunction of surfactant in preterm infants is due to lung immaturity.
感染阿留申水貂病细小病毒（ADV）的新生水貂幼崽会患上急性间质性肺炎，其临床症状和病理损伤与患有呼吸窘迫综合征的早产人类婴儿以及患有成人呼吸窘迫综合征的成人相似。我们之前曾提出ADV在肺的II型肺泡上皮细胞中复制。通过使用双重原位杂交，同时使用一个探针检测ADV复制以及一个探针显示II型肺泡细胞，我们现在证实了这一假设。此外，Northern（RNA）印迹杂交显示，该感染导致II型肺泡细胞产生的表面活性物质相关蛋白C mRNA显著减少。因此，我们认为在感染ADV的水貂幼崽中观察到的以透明膜形成为特征的严重临床症状和病理变化是由肺泡表面活性物质功能障碍引起的，这与早产婴儿呼吸窘迫综合征中观察到的情况相似。然而，在受感染的水貂幼崽中，这种功能障碍是由于ADV在肺部的复制，而早产婴儿中表面活性物质的功能障碍是由于肺不成熟。
